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Influence of pharmacological and epigenetic factors to suppress neurotrophic factors and enhance neural plasticity in stress and mood disorders

机译:药理和表观遗传因素在压力和情绪障碍中抑制神经营养因子并增强神经可塑性的影响

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摘要

Induced stress factors deregulate the structural remodelling of brain considering synaptic modifiers such as neurotropins and glucocorticoids disrupt the cognitive ability and decreases the DLPFC and VmPFC region functioning ( ). Neural plasticity occurs, due to dysregulation in the pre- and post-synaptic neural receptor modelling, due to oxidative stress: in which unwanted oxidation of ions causes malfunctioning of transcription process resulting in genetic variation. Due to pharmacological and environmental factors:several drugs-abuses (like cocaine) affects synaptic NAc MSN excitability, resulting in the development and expression of addictive plasticity as receptors becomes familiar to these external agents and overgeneralize them as self or natural pathway mediator
机译:考虑到诸如神经营养蛋白和糖皮质激素的突触修饰剂破坏了认知能力并降低了DLPFC和VmPFC区域的功能,诱导的压力因子使大脑的结构重塑失调。由于突触之前和之后的神经受体建模失调,以及由于氧化应激,都会发生神经可塑性:在这种情况下,离子的有害氧化会导致转录过程出现功能异常,从而导致遗传变异。由于药理和环境因素:多种药物滥用(如可卡因)会影响突触NAc MSN兴奋性,导致成瘾性可塑性的产生和表达,因为受体已被这些外部因子所熟悉并过度概括为自身或天然途径介体

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